Preparedness for a natural disaster: how Coriell planned for hurricane Sandy.

When a biological specimen is donated to a biobank such as the nonprofit Coriell Institute for Medical Research, regardless of whether that submission is sent directly or through a physician, scientist, foundation, or patient-centered advocacy organization, the donor expects their biomaterial to be processed effectively and stored in proper conditions until distribution to researchers answering scientific questions. The donor and scientific researchers rarely, if ever, consider what might happen to those specimens if the biobank experiences an adverse event, such as a disaster that compromises its business operations, including handling of samples. Management of biomaterials is not simply a laboratory process; their long-term survival is dependent on both the laboratory preparation and the infrastructure designed for maintenance, safety, and security. Coriell Institute has documented disaster preparedness plans since its inception in 1953, and currently manages hundreds of thousands of cell lines and DNA samples under ISO 9001 quality management standards, complete with a robust Emergency Operations Plan. The Institute's recent approach to preparing for Hurricane Sandy, a Category 1 hurricane that struck the East Coast of the United States in late October 2012, was two-fold. It included the validation of its long-term strategies focused on emergency back-up systems, communication solutions, and employee training, and implementation of short-term tactics such as confirming on-call emergency response personnel and safe storage options for working biomaterials and reagents. The purpose of this article is to review several best practices in use at Coriell Institute associated with disaster planning and to identify and evaluate the effectiveness of those elements in coping with Hurricane Sandy.

Dysmyelination and reduced myelin basic protein gene expression by oligodendrocytes of SHP-1-deficient mice.

We have shown previously that myelin-forming oligodendrocytes express the protein tyrosine phosphatase SHP-1 and that myelin formation was decreased in SHP-1-deficient motheaten mice compared to that in normal littermates. These studies suggested a potential importance for SHP-1 in oligodendrocyte and myelin development. To address further this possibility, we analyzed myelin formation by microscopy and myelin basic protein (MBP) gene expression in motheaten mice at ages when myelination occurs in the developing central nervous system (CNS). Furthermore, we correlate these findings with MBP gene expression in oligodendrocytes grown in vitro. We have found that CNS myelination was significantly reduced in SHP-1-deficient mice relative to their normal littermates at multiple times during the active period of myelination. Under electron microscopy, greater numbers of axons in spinal cords of motheaten mice were either unmyelinated or had thinner myelin sheathes compared to those in matched areas of normal littermates. Accordingly, MBP protein and mRNA levels were reduced in SHP-1-deficient mice compared to that in the CNS of normal littermates. In vitro, O1(+) oligodendrocytes from motheaten mice expressed much less MBP than O1(+) oligodendrocytes of normal littermates indicating an alteration in oligodendrocyte differentiation. The latter correlated with reduced MBP mRNA relative to cerebroside galactosyl transferase (CGT) gene mRNA in SHP-1-deficient oligodendrocytes in purified cultures. We propose that SHP-1 is a critical regulator of developmental signals leading to terminal differentiation and myelin sheath formation by oligodendrocytes.